Regulation of renal water excretion is controlled by antidiuretic hormone (ADH) and renal sodium excretion is regulated, in part, by renin secretion. Recent investigations have indicated that a group of cellular hormones, prostaglandins, may be involved in modulating the renal water retaining effects of ADH, in promoting natriuresis in the distal nephron, and in renal baroreceptor and beta-adrenergic control of renin release. The objectives of the proposed studies are as follows: 1) To determine if basal and stimulated rates of renal prostaglandin synthesis are significantly involved in determining the renal response to plasma ADH concentrations within the normal physiological range for this hormone. This will be done by correlating measurements of plasma ADH concentration, renal PGE2 excretion and renal water and excretion with basal, stimulated and inhibited rates of renal PGE2 synthesis. 2) To determine if plasma levels of ADH less than that required to maximally concentrate the urine are capable of producing significant increases in renal sodium excretion and to determine if ADH stimulated natriuresis is related to increased renal prostaglandin synthesis. These studies will be conducted in conscious dogs in which measurements of plasma ADH concentration will be correlated with renal PGE2 and electrolyte excretion before and during continuous infusions of synthetic arginine vasopressin. 3) Studies in acutely prepared, anesthetized dogs will be done to determine if macula densa control of renin secretion, ADH inhibition of renin secretion, or the negative feedback inhibition by angiotensin II of renin secretion invokes renal cortical prostaglandin synthesis as an intermediary mechanism. The overall objective of these experiments is to further delineate hormonal mechanisms concerned with regulation of extracellular fluid volume and blood pressure.